Despite long-standing recognition of sensory symptoms in autism, few empirical studies have examined the nature and specificity of dysfunction in this domain. The extant research demonstrates that sensory dysfunction is very significant clinical problem in autism, and may furthermore be related to the presence or development of other behavioral and social deficits. Within the domain of chemosensory processing, there is considerable evidence that children with autism show unusual responses to tastes and odors, and we have recently documented autism-specific impairments in psychophysiological tests of taste and odor identification. Taste and smell are both critical for ingestive behaviors, and a growing literature documents high rates of restricted and atypical eating in children with autism. Olfaction is also critical in mammalian social identification. Research in schizophrenia, and more recently our work in autism, has found a link between impaired odor identification and social dysfunction. Both taste and olfactory functions have been shown to aggregate in non-autism families, and familiality has also been found for some of the food preference, behavioral, and social symptoms that we hypothesize are related to chemosensory deficits. In this project, we shall further investigate chemosensory processing in autism and how it is related to feeding and social behaviors, and the familiality of these quantitative traits. In Aim 1, we shall phenotype 175 families (including a proband with autism, an unaffected sibling, and both parents), and 100 well-matched typical controls, on their ability to detect and identify odorants and tastes, pattern of food preferences, and degree of social impairment. In Aim 2, we shall determine autism-specific patterns of chemosensory and related functions, and examine how these quantitative traits are interrelated. In Aim 3, we shall determine the familial aggregation of these traits. Taken together this work will provide new frameworks for understanding sensory deficits in autism spectrum disorders and how these quantitative traits can serve as markers for increased liability to ASDs.